详细内容（前10条）

1. ⭐ GSE333464 PLA2G2D 在肿瘤引流淋巴结中调节抗肿瘤免疫

• ✍️ 作者：未知作者
• 🏷️ 关键词：immunity、lymph、regex:lymph(o|atic)?
• 📝 描述：Contributors : Anneloes van Krimpen ; Mike Eterman ; Menno van Nimwegen ; Ralph Stadhouders ; Floris DammeijerSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusCurrent cancer immunotherapies can induce tumour regression, although responses are often not durable. Recent studies have highlighted the importance of enforcing a systemic immune response from tumour-draining lymph nodes (TDLNs). However, mechanisms driving immune suppression in TDLNs remain poorly studied. We applied spatial proteogenomics on melanoma TDLNs and identified regional differences in immune cell composition in lymph nodes from patients with long-term (>5 years) disease control compared to those with early (<2 years) disease recurrence. TDLNs from patients with a poor prognosis were characterized by the expansion of regulatory T cells (Tregs), dendritic cells (DCs), and macrophages interacting with cytotoxic CD8+ T cells. Targeted transcriptomics of cell types within this spatial neighbourhood revealed immunoregulatory myeloid cell phenotypes engaging with CD8+ T cells poised for exhaustion. Besides known immune-suppressive molecules such as IDO and PD-L1, paracortex macrophages and DCs in patients with recurrent disease expressed high levels of the secreted phospholipase PLA2G2D across different cancer types. Additionally, PLA2G2D was upregulated in non-small cell lung cancer patients who developed acquired resistance to anti-PD-1 immunotherapy. Importantly, PLA2G2D loss-of-function or therapeutic inhibition markedly improved survival in tumour-bearing mice and increased the efficacy of anti-PD-1 immunotherapy. Collectively, we show that in-depth spatial profiling of cancer patient TDLNs offers novel insights into systemic anti-tumour immunity and identifies PLA2G2D as a target for cancer immunotherapy.
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2. ⭐ GSE314885 同基因小鼠模型中 7 × 19 CAR-T 细胞给药诱导的受体免疫细胞的基因表达谱分析 [scRNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、T cell、scRNA
• 📝 描述：Contributors : Yo Muraki ; Yuumi Okuzono ; Rina Kurisu ; Akiko Abiru ; Yukimi Sakoda ; Koji Tamada ; Chihiro AkimotoSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusChimeric antigen receptor (CAR)-T cell therapy is effective for hematologic malignancies; however, the response of solid tumors is limited because of the immunosuppressive tumor microenvironment, antigen heterogeneity, and lack of persistence of transferred T cells. To overcome these challenges, CAR-T cells expressing interleukin-7 and chemokine (C-C motif) ligand 19 (7 × 19 CAR-T) were generated to achieve potent antitumor efficacy through the recruitment and proliferation of CAR-T cells and endogenous immune cells. To elucidate the underlying mechanism of 7 × 19 CAR-T cells against solid tumors, we analyzed the cellular composition and gene expression profiles of host immune cells following CAR-T cell infusion in a murine solid tumor model. Antihuman CD20 7 × 19 CAR-T cells were prepared using Thy 1.1 congenic mice and administered to C57BL/6N mice bearing subcutaneous MC38 tumors expressing human CD20. The tumors were harvested 4 days postinfusion to capture early immune responses before overt tumor regression. CD90.1- recipient immune cells were subjected to flow cytometry analysis, and transcriptomics changes were determined using AmpliSeq and single-cell RNA seq. An increase in recipient CD8+ T cells and macrophages was observed in the tumor of mice treated with 7 × 19 CAR-T cells, but not with conventional CAR-T. The expression of chemokines and genes associated with the inflammatory pathway was upregulated only in recipient immune cells of the 7 × 19 CAR-T-treated mice. Single-cell RNA-seq analysis revealed upregulation of pro-inflammatory genes and chemokines in the dendritic cell and monocyte/macrophage populations. These results indicate that 7 × 19 CAR-T cells initiate the early recruitment and activation of host immune cells, which contributes to their superior antitumor activity compared with conventional CAR-T cells.
• 🔗 查看原文

3. ⭐ GSE282437 PLA2G2D 在肿瘤引流淋巴结中调节抗肿瘤免疫

• ✍️ 作者：未知作者
• 🏷️ 关键词：immunity、lymph、regex:lymph(o|atic)?
• 📝 描述：Contributors : Anneloes van Krimpen ; Ralph Stadhouders ; Floris Dammeijer ; Anne OnrustSeries Type : OtherOrganism : Homo sapiensCurrent cancer immunotherapies can induce tumor regression, although responses are often not durable for reasons that are incompletely understood. Apart from activating pre-existing tumor-infiltrating T cells, recent studies have highlighted the importance of enforcing a systemic immune response from tumor-draining lymph nodes (TDLNs). However, mechanisms driving immune suppression in TDLNs remain poorly studied. We applied spatial proteogenomics on melanoma TDLNs and identified striking regional differences in immune cell composition in lymph nodes from patients with long-term (>5 years) disease control compared to those with early (<2 years) disease recurrence. TDLNs from patients with a poor prognosis were characterized by the expansion of a specific cellular interaction network in the lymph node paracortex, consisting of regulatory T cells (Tregs), dendritic cells (DCs) and macrophages interacting with cytotoxic CD8+ T cells. Targeted transcriptomics of cell types within this spatial neighbourhood revealed immunoregulatory myeloid cell phenotypes engaging with CD8+ T cells poised for exhaustion. Macrophages in patients with early disease recurrence resided in a dysfunctional state bearing hallmarks of chronic interferon-signalling – frequently residing near CD8+ T-cell–DC dyads. Besides known immune-suppressive molecules such as IDO and PD-L1, paracortex macrophages and DCs in patients with recurrence expressed high levels of the secreted phospholipase PLA2G2D across different cancer types. In addition, PLA2G2D was upregulated in non-small cell lung cancer patients upon acquired resistance to anti-PD-1 immunotherapy. Importantly, PLA2G2D loss-of-function or therapeutic inhibition markedly improved survival in tumor-bearing mice and increased the efficacy of anti-PD-1 immunotherapy. Collectively, we show that in-depth spatial profiling of cancer patient TDLNs offers novel insights into systemic anti-tumor immunity and identifies PLA2G2D as a target for cancer immunotherapy.
• 🔗 查看原文

4. GSE329895 双逆转录酶免疫系统协调合成双链DNA [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、RNA-seq
• 📝 描述：Contributors : Megan Wang ; Kanta Yoneyama ; Rimantė Žedaveinytė ; Junichiro Ishikawa ; Stephen Tang ; Hoang C Le ; Tanner Wiegand ; Josephine L Ramirez ; Naoto Nagahata ; Yanzhe Ma ; Dennis J Zhang ; Erick Helmeczi ; Mirela Berisa ; Marko Jovanovic ; Masahiro Hiraizumi ; Keitaro Yamashita ; Hiroshi Nishimasu ; Samuel H SternbergSeries Type : Expression profiling by high throughput sequencingOrganism : Escherichia coliRecent studies have revealed that defense-associated reverse transcriptase (DRT) systems mediate antiviral immunity through distinct modes of cDNA synthesis. Class I DRTs catalyze untemplated DNA synthesis with random or nucleotide-biased sequences, whereas Class II DRTs polymerize noncoding RNA-templated products, including concatemeric repeats and homopolymeric cDNA. However, how these distinct modes of cDNA synthesis are employed to drive antiviral defense remains poorly understood. Here, we report a distinctive mechanism of DRT3 immunity, in which RT enzymes from both Class I and Class II coordinate their diverse activities to produce self-complementary double-stranded DNA (dsDNA). Remarkably, whereas the DRT3a enzyme relies on a 5′-ACACAC-3′ RNA template to synthesize long poly-(dTdG) repeats, DRT3b synthesizes precise poly-(dCdA) repeats without any nucleic acid template at all. The cryo-electron microscopy structure reveals that DRT3b assembles into a hexameric complex and employs active site-adjacent residues to function as deoxyadenosine and deoxycytidine gates that enforce alternating addition to produce dinucleotide repeats, representing a unique example of amino acid-templated DNA polymerization. Strikingly, DRT3 immune systems are toxic in a genetic background lacking E. coli RecBCD, implicating host recombination machinery in limiting DRT3-mediated dsDNA levels. Consistent with this model, we discovered that the phage-encoded RecBCD inhibitor, Gam, potently triggers DRT3-mediated abortive infection. Collectively, our findings reveal how two polymerases with distinct templating strategies cooperate to generate complementary DNA and drive antiviral defense.
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5. GSE303716 Nodal/Smad2 信号通过抑制 Pparg 介导的脂质代谢来维持发育停滞 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolism、RNA-seq
• 📝 描述：Contributors : Giacomo Furlan ; Evelyne Collignon ; Miguel Ramalho SantosSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusCells and organisms can enter transient dormant states to survive unfavorable conditions during development, physiological adult states and disease. One paradigmatic case of dormancy is diapause, whereby embryos transiently pause development and enter a state of suspended animation. In mammals, diapause occurs pre-implantation at the blastocyst state and involves global growth suppression and metabolic rewiring towards lipid usage as energy source. The molecular regulation of diapause remains poorly understood, including whether it occurs by default or requires active signaling. Here, we identify the canonical TGF-β signaling pathway as an essential driver of transcriptional and metabolic reprogramming in diapause. TGF-β signaling was thought to only be required post-implantation, but we show that the ligand Nodal and its downstream effector Smad2 are essential for the survival of paused embryonic stem cells (ESCs) and blastocysts. Mechanistically, we found that Smad2 represses a Pparg, a transcription factor that is a master regulator of lipid storage, a process incompatible with pausing. Ablation of Pparg in Smad2-deficient ESCs rescues their survival and prevents excess lipid buildup in pausing conditions. These findings establish Nodal/Smad2 signaling as pivotal for sustaining embryonic diapause and suggest that the crosstalk between TGF-β signaling and the Pparg pathway may be broadly relevant for metabolic rewiring in dormancy contexts.
• 🔗 查看原文

6. GSE302996 Nodal/Smad2 信号通过抑制 Pparg 介导的脂质代谢来维持发育停滞 [ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolism、ATAC-seq
• 📝 描述：Contributors : Giacomo Furlan ; Evelyne Collignon ; Miguel Ramalho SantosSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusCells and organisms can enter transient dormant states to survive unfavorable conditions during development, physiological adult states and disease. One paradigmatic case of dormancy is diapause, whereby embryos transiently pause development and enter a state of suspended animation. In mammals, diapause occurs pre-implantation at the blastocyst state and involves global growth suppression and metabolic rewiring towards lipid usage as energy source. The molecular regulation of diapause remains poorly understood, including whether it occurs by default or requires active signaling. Here, we identify the canonical TGF-β signaling pathway as an essential driver of transcriptional and metabolic reprogramming in diapause. TGF-β signaling was thought to only be required post-implantation, but we show that the ligand Nodal and its downstream effector Smad2 are essential for the survival of paused embryonic stem cells (ESCs) and blastocysts. Mechanistically, we found that Smad2 represses a Pparg, a transcription factor that is a master regulator of lipid storage, a process incompatible with pausing. Ablation of Pparg in Smad2-deficient ESCs rescues their survival and prevents excess lipid buildup in pausing conditions. These findings establish Nodal/Smad2 signaling as pivotal for sustaining embryonic diapause and suggest that the crosstalk between TGF-β signaling and the Pparg pathway may be broadly relevant for metabolic rewiring in dormancy contexts.
• 🔗 查看原文

7. GSE302766 Nodal/Smad2 信号通过抑制 Pparg 介导的脂质代谢来维持发育停滞 [ATAC-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolism、ATAC-seq
• 📝 描述：Contributors : Furlan Giacomo ; Collignon Evelyne ; Ramalho Santos MiguelSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusCells and organisms can enter transient dormant states to survive unfavorable conditions during development, physiological adult states and disease. One paradigmatic case of dormancy is diapause, whereby embryos transiently pause development and enter a state of suspended animation. In mammals, diapause occurs pre-implantation at the blastocyst state and involves global growth suppression and metabolic rewiring towards lipid usage as energy source. The molecular regulation of diapause remains poorly understood, including whether it occurs by default or requires active signaling. Here, we identify the canonical TGF-β signaling pathway as an essential driver of transcriptional and metabolic reprogramming in diapause. TGF-β signaling was thought to only be required post-implantation, but we show that the ligand Nodal and its downstream effector Smad2 are essential for the survival of paused embryonic stem cells (ESCs) and blastocysts. Mechanistically, we found that Smad2 represses a Pparg, a transcription factor that is a master regulator of lipid storage, a process incompatible with pausing. Ablation of Pparg in Smad2-deficient ESCs rescues their survival and prevents excess lipid buildup in pausing conditions. These findings establish Nodal/Smad2 signaling as pivotal for sustaining embryonic diapause and suggest that the crosstalk between TGF-β signaling and the Pparg pathway may be broadly relevant for metabolic rewiring in dormancy contexts.
• 🔗 查看原文

8. GSE333855 RNY1 分布于细胞外囊泡和核糖核蛋白颗粒中，并在炎症期间通过气道液调节巨噬细胞的编程。

• ✍️ 作者：未知作者
• 🏷️ 关键词：macrophage、inflammation
• 📝 描述：Contributors : Cherie E Saffold ; Antiana C Richardson ; Heather H PuaSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusYRNAs are small noncoding RNAs that are abundant in the extracellular space. Prior research has shown that YRNAs are present in most biofluids and that their levels fluctuate during disease. Yet our understanding of YRNA dynamics in the context of biofluid extracellular particles during disease processes is limited. In this study, we found that RNY1, one of two murine YRNAs, increases in airway fluid during allergen-induced lung inflammation and correlates with neutrophil infiltration. Using RNase sensitivity assays and size exclusion chromatography, we determined that airway fluid RNY1 is protected by both EVs and protein-containing structures in distinct extracellular compartments. In contrast the other murine YRNA, RNY3, is only enriched in BALF EVs, suggesting that RNY1 is uniquely partitioned in heterogenous extracellular particles. Both EV-enriched and protein-enriched RNY1-containing extracellular compartments were able program robust pro-inflammatory transcriptional responses in target macrophages. RNY1 contributed to this programming, as macrophages treated with a protein-enriched compartment isolated from RNY1-/- mice demonstrated lower induction of interferon-associated genes. Together, this study demonstrates that YRNAs are heterogeneously packaged in complex biofluids and contribute to intercellular signaling axes during inflammation.
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9. GSE307266 对衰老肠道分泌组的定量表征揭示了在细胞外空间发挥作用以调节寿命的新型分泌蛋白

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging、regex:intestin(e|al)
• 📝 描述：Contributors : Jason Wayne Miklas ; Daniel Joseph Richard ; Brandon Ameglio ; Anne BrunetSeries Type : Expression profiling by high throughput sequencingOrganism : Caenorhabditis elegansSecreted proteins are essential to modulate the extracellular space and communicate to distal cells or tissues. But the importance of extracellular proteins in aging has been understudied. Here we use proximity labeling followed by quantitative proteomics to systematically characterize the intestine and neuron secretome in C. elegans. We identify many previously unknown intestine secreted proteins that change with age, and we validate the secretion of these proteins by in vivo cell biology. One of these secreted proteins, ACP7, is well conserved in humans. Overexpressing ACP7 extends lifespan in a secretion-dependent manner, and we find that ACP7 acts as a phosphatase in the extracellular space. Finally, we identify additional proteins along the secretion pathway that regulate lifespan, including VAPA – a protein localized to small secretory vesicles in the intestine. Our systematic characterization of tissue-specific secretome during aging uncovers novel proteins that impact lifespan and highlights the role of extracellular enzymes in aging.
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10. GSE313034 同基因小鼠模型中 7 × 19 个 CAR-T 细胞给药诱导的受体免疫细胞基因表达谱分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、T cell
• 📝 描述：Contributors : Yo Muraki ; Yuumi Okuzono ; Rina Kurisu ; Akiko Abiru ; Yukimi Sakoda ; Koji Tamada ; Chihiro AkimotoSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusChimeric antigen receptor (CAR)-T cell therapy is effective for hematologic malignancies; however, the response of solid tumors is limited because of the immunosuppressive tumor microenvironment, antigen heterogeneity, and lack of persistence of transferred T cells. To overcome these challenges, CAR-T cells expressing interleukin-7 and chemokine (C-C motif) ligand 19 (7 × 19 CAR-T) were generated to achieve potent antitumor efficacy through the recruitment and proliferation of CAR-T cells and endogenous immune cells. To elucidate the underlying mechanism of 7 × 19 CAR-T cells against solid tumors, we analyzed the cellular composition and gene expression profiles of host immune cells following CAR-T cell infusion in a murine solid tumor model. Antihuman CD20 7 × 19 CAR-T cells were prepared using Thy 1.1 congenic mice and administered to C57BL/6N mice bearing subcutaneous MC38 tumors expressing human CD20. The tumors were harvested 4 days postinfusion to capture early immune responses before overt tumor regression. CD90.1- recipient immune cells were subjected to flow cytometry analysis, and transcriptomics changes were determined using AmpliSeq and single-cell RNA seq. An increase in recipient CD8+ T cells and macrophages was observed in the tumor of mice treated with 7 × 19 CAR-T cells, but not with conventional CAR-T. The expression of chemokines and genes associated with the inflammatory pathway was upregulated only in recipient immune cells of the 7 × 19 CAR-T-treated mice. Single-cell RNA-seq analysis revealed upregulation of pro-inflammatory genes and chemokines in the dendritic cell and monocyte/macrophage populations. These results indicate that 7 × 19 CAR-T cells initiate the early recruitment and activation of host immune cells, which contributes to their superior antitumor activity compared with conventional CAR-T cells.
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1. RNA测序揭示了拟南芥花序分生组织细胞命运的新见解

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing
• 📝 描述：RNA sequencing of individual nuclei revealed how stem cells in the Arabidopsis inflorescence meristem commit to distinct developmental fates and establish tissue patterning earlier than previously recognized… The post RNA sequencing reveals new insights into the cell fates of the Arabidopsis inflorescence meristem appeared first on RNA-Seq Blog.
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• GSE336086 线粒体 STAT3 介导的细胞凋亡抑制限制抗分枝杆菌免疫
• GSE336034 巨噬细胞增强靶向嵌合体用于细胞外蛋白降解
• GSE335846 RNA-seq 分析了奥希替尼处理的 PC9 细胞在特定细胞周期阶段的情况
• GSE335244 髓系 MMP14 将细胞外蛋白水解与肥胖期间的炎症和代谢重塑联系起来
• GSE330641 双逆转录酶免疫系统协调合成双链DNA [miniprep-seq]
• GSE330639 双逆转录酶免疫系统协调合成双链DNA [cDIP-seq]
• GSE329897 双逆转录酶免疫系统协调合成双链DNA [RIP-seq]
• GSE329894 双逆转录酶免疫系统协调合成双链DNA [Tn-seq]
• GSE328604 DICER1相关肿瘤易感突变导致3p-miRNA功能增强、HERVH活性增强以及转移潜能增加
• GSE325557 核小体重塑因子在酵母中去保护端粒切除过程中的作用 [ChIP-seq]
• GSE318738 氮胁迫和水分胁迫下玉米B73和ZmCCD8突变体的比较转录组学研究
• GSE313554 TRPM4 表达作为前列腺癌中乙酰西酞普兰活性的预测生物标志物和机制驱动因素：临床前疗效研究。
• GSE303541 确定四种检测方法与心脏移植中抗体介导的排斥反应之间的关系
• GSE301334 FSGS斑马鱼损伤模型中转录组、miRNA和选择性剪接的调控
• GSE284462 转座元件驱动的增强子 RNA 库扩张是谷类作物调控创新和多倍体适应的基础 [PolyA RNA-seq]
• GSE284461 转座元件驱动的增强子 RNA 库扩张是谷类作物调控创新和多倍体适应的基础 [CB RNA-seq]
• GSE284460 转座元件驱动的增强子 RNA 库扩张是谷类作物调控创新和多倍体适应的基础 [ChIP-seq]
• GSE284038 Argonaute 蛋白调控精子发生转录程序的时序 [scRNA-seq]
• GSE284037 Argonaute 蛋白调控精子发生转录程序的时序 [RNA-seq]
• GSE283114 黏连蛋白和NuRD通过PLZF拮抗性地驱动不同的神经元命运
• GSE276607 逆转录转座元件沉默因子 Daxx 控制成年大脑中小胶质细胞的特性和功能 [RNA-seq]
• GSE267028 逆转录转座元件沉默因子 Daxx 控制成年大脑中的小胶质细胞特性和功能 [ATAC-seq]
• GSE247372 Myc 维持果蝇肠道中区域性和性别二态性脂质稳态
• GSE206076 ZNF512B 保护关键调控区域，以维护基因组的长期完整性。[scRNA-Seq]
• GSE206071 ZNF512B 保护关键调控区域，以维护基因组的长期完整性。[RNA-Seq]
• GSE319321 一份来自两个季节时间点采集的 Orestias ascotanensis 多种组织的 RNA 测序数据集
• GSE336083 一项全口服方案 CC-486 和维奈托克治疗急性髓系白血病的 1/1b 期研究
• GSE335990 免疫复合物上迁移的SlanMo基因表达
• GSE335824 评估白蛋白与晶体液在脓毒症复苏中免疫反应的差异
• GSE335637 肿瘤来源的外泌体 METTL3 通过 m6A–IGF2BP2–ATG2A 轴重编程巨噬细胞，促进肺腺癌干细胞特性和脑转移
• GSE335382 肿瘤抑制候选基因3参与小鼠存活、颅面和皮层发育
• GSE334857 CD4⁺ T 细胞失调与新冠长期症状：来自未接种疫苗人群的启示
• GSE300510 AP-1介导的谱系记忆塑造人类皮肤中的病毒抵抗屏障
• GSE331310 建立和验证NEX-RiboTag系统用于分析出生后小鼠前脑兴奋性神经元翻译组
• GSE301536 肺分支形态发生和上皮谱系分化的类器官模型 [BLO scRNA-seq]
• GSE300724 肺分支形态发生和上皮谱系分化的类器官模型 [scRNA-Seq]
• GSE300722 肺分支形态发生和上皮谱系分化的类器官模型[RNA-Seq]
• GSE300130 利用雄激素受体细胞周期效应增强 CDK4/6 抑制剂在雌激素受体阳性转移性乳腺癌中的疗效
• GSE281570 RNA-seq 研究，使用 Karpas422 异种移植瘤，分别在载体或 PRC2 抑制剂 C36 处理后进行。